Gastroprotective effect of vanadium in rats - the roles of gastric acid and nitric oxide

  • T.P. Omayone
  • A.T. Salami
  • F.S. Oluwole
  • S.B. Olaleye
Keywords: Sodium Metavanadate, Gastric Ulcer, Gastric Acidity, Oxidative Stress, Nitric Oxide

Abstract

Vanadium (various forms) has been proven to be beneficial in the treatment of certain diseases, especially diabetes. Reports have it that vanadium may protect the stomach from gastric ulcerogens such as ethanol and acid. This study was designed to investigate the probable mechanism Vanadium exerts its’ gastroprotective activities.

Methods: Sodium metavanadate (0, 5, 10 and 20 mg/kg. p.o) was administered to 20 male Wistar rats weighing (150±20g) for two weeks. Gastric ulcer was induced using ethanol after which animals were sacrificed 2 hours later. In study two, 30 male Wistar rats (114±10g) were administered sodium metavanadate at (0, 50 and 200 ppm) in drinking water for 10weeks after which ulcer was induced using pylorus ligation method. Basal and histamine (10mg/kg i.m) stimulated gastric secretions were determined through continuous perfusion technique afterwards in un-ulcerated animals. Ulcer score, mucin content, gastric nitrite level, anti-oxidant and H+K+ATPase activities were investigated in gastric homogenate samples.

Results: Sodium metavanadate significantly reduced ulcer index and MDA levels while enhancing NO concentrations, catalase and SOD activities in both method of gastric ulceration. Mean basal gastric output was not significantly different in control compared with 50 and 200 ppm V group. Stimulation with histamine caused significant increases in gastric output by 187.72%, 57.40% and 78.69% in control, 50 and 200 ppm V respectively and was significantly reduced in the vanadium treated groups. A significant decrease in H+K+ ATPase (proton) pump activities of the vanadium exposed groups compared with control in the pylorus ligation ulcer model was observed.

Conclusion: Vanadium may be suggested to have protective activities against gastric ulceration by acting as a proton pump inhibitor, enhancing anti-oxidant enzyme activities as well as mucosal blood flow via increased NO mechanism.

Keywords: Sodium Metavanadate, Gastric Ulcer, Gastric Acidity, Oxidative Stress, Nitric Oxide

Published
2016-08-17
Section
Articles

Journal Identifiers


eISSN: 2449-108X
print ISSN: 2315-9987